Cirrhosis and Chronic Liver Failure:

Part I. Diagnosis and Evaluation

JOEL J. HEIDELBAUGH, M.D., and MICHAEL BRUDERLY, M.D.
University of Michigan Medical School, Ann Arbor, Michigan

Cirrhosis and chronic liver failure are leading causes of morbidity and mortality in the United States, with the majority of
preventable cases attributed to excessive alcohol consumption, viral hepatitis, or nonalcoholic fatty liver disease. Cirrho-
sis often is an indolent disease; most patients remain asymptomatic until the occurrence of decompensation, character-
ized by ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, or variceal bleeding from portal hypertension.
Physical examination of patients with cirrhosis may reveal a variety of findings that necessitate a hepatic- or gastro-
intestinal-based work-up to determine the etiology. Some patients
already may have had laboratory or radiographic tests that incidentally
uncovered signs of cirrhosis and its comorbidities. No serologic or
radiographic test can accurately diagnose cirrhosis. A significant corre-
lation has been demonstrated between persistently elevated liver func-
tion tests and biopsy-proven underlying hepatic disease; thus, a more
targeted serologic work-up is indicated in patients whose liver function
test results are persistently abnormal. Unnecessary medications and
surgical procedures should be avoided in patients with cirrhosis. Refer-

ILLUSTRATION BY FLOYD E. HOSMER

ral for liver biopsy should be considered only after a thorough, non-
invasive serologic and radiographic evaluation has failed to confirm a
diagnosis of cirrhosis; the benefit of biopsy outweighs the risk; and it
is postulated that biopsy will have a favorable impact on the treatment
of chronic liver disease. (Am Fam Physician 2006;74:756-62,781. Copy-
right © 2006 American Academy of Family Physicians.)

C
This is part I of a two-part irrhosis and chronic liver fail- as nonalcoholic steatohepatitis, or NASH)
article on cirrhosis and
ure together were the 12th most is an increasingly common cause of liver
chronic liver failure.
Part II, “Complications common cause of death in the injury; risk factors include obesity, diabetes,
and Treatment,” appears United States in 2002, accounting hypertriglyceridemia, and profound weight
in this issue of AFP on for 27,257 deaths (9.5 per 100,000 persons), loss after jejunoileal bypass.5
page 767.
with a slight male predominance.1 Approxi- According to estimates from the United
Patient information:
S

A handout on cirrhosis and
chronic liver failure, writ-
ten by the authors of this
article, is on page 781.
mately 40 percent of patients with cirrhosis
are asymptomatic, and the condition often
is discovered during a routine examination
with laboratory or radiographic studies, or at
autopsy. In 2000, there were 360,000 U.S. hos-
pital discharges related to cirrhosis and liver
failure.1 This article, part I of a two-part series,
outlines the diagnosis and evaluation of cir-
rhosis and chronic liver failure (Figure 1). Part
II discusses complications and treatment.2
Single or multifactorial insults to the liver
ultimately lead to cirrhosis, the most com-
mon being alcohol abuse, chronic hepatitis C,
and obesity with concomitant nonalcoholic
fatty liver disease (Table 1).3,4 Nonalcoholic
fatty liver disease (NAFLD; formerly known
Network for Organ Sharing, 75 to 80 per-
cent of cirrhosis cases could be prevented by
eliminating alcohol abuse, and approximately
3.9 million Americans have chronic hepati-
tis C.6 In August 2005, there were 17,935 per-
sons with cirrhosis (from various etiologies)
in the United States who were awaiting a liver
transplant.6 Mortality rates in patients with
alcoholic liver disease are considerably higher
than in patients with other forms of cirrhosis.
The Centers for Disease Control and Preven-
tion estimates that 75,766 deaths and 2.3 mil-
lion years of potential life lost during 2001
were attributable to excessive alcohol use, an
average of approximately 30 years of potential
life lost for each alcohol-attributable death.7

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 SORT: KEY RECOMMENDATIONS FOR PRACTICE

Evidence
Clinical recommendation rating References

Although no laboratory test can diagnose cirrhosis accurately, liver function tests, a complete blood count C 14
with platelets, and a prothrombin time test should be performed if a liver abnormality is suspected.
If clinical, laboratory, and radiographic data are inconclusive, but suspicion of cirrhosis remains, C 15, 17
a diagnostic liver biopsy should be performed.
If serum transaminase levels are greater than twice the upper limit of normal or remain elevated for C 15
longer than six months, additional serologic studies should be performed to evaluate for various
etiologies of cirrhosis. If clinical suspicion for liver disease is high, further serologic work-up is
warranted earlier.
Abdominal ultrasonography is a specific, reliable, noninvasive, fast, and cost-effective test that C 20, 21
should be used as a first-line radiographic study for diagnosing cirrhosis.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-
oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 699 or
http://www.aafp.org/afpsort.xml.

Diagnosis of Cirrhosis and Chronic Liver Failure

History:
Patient presents with signs and
symptoms of chronic liver disease
or has risk factors for chronic liver
disease (e.g., alcohol abuse, risk
of viral hepatitis, obesity).
Physical examination:
Patient has hallmark
findings consistent with
chronic liver disease
(see Table 2).
Laboratory studies:
Patient has incidental liver panel*
abnormalities (e.g., elevated ALT and/
or AST) or positive screen for serologic
markers of liver disease (see Table 3).
Radiographic studies:
Patient has incidental findings
suggestive of liver disease on
routine studies (e.g., abdominal
ultrasonography, CT, MRI).

Physical examination findings
consistent with liver disease
(see Table 2) or high suspicion
for chronic liver disease
Confirm history via signs
and symptoms of chronic
liver disease and positive risk
factors (e.g., alcohol abuse,
risk of viral hepatitis, obesity).
Confirm history via signs and symptoms of
chronic liver disease and positive risk factors
(e.g., alcohol abuse, risk of viral hepatitis,
obesity) and screen for hallmark physical
examination findings (see Table 2).

Obtain liver panel* (if not already obtained), CBC with platelets, prothrombin
time, and targeted serologic studies to determine etiology of cirrhosis,
highlighting risk factors and family history for liver disease (see Table 3).

Obtain abdominal ultrasonography with Doppler (if not already performed) to evaluate
for morphologic abnormalities consistent with cirrhosis and to assess for potential
complications (e.g., ascites, varices, portal hypertension, portal vein thrombosis).

Refer for possible liver biopsy if diagnosis of cirrhosis is uncertain, as well as

possible determination of etiology via histology if not readily determinable
through serologic testing and if potential benefit outweighs risk of procedure.

*—Tests included in standard liver panels vary but typically include the serum enzymes ALT, AST, alkaline phosphatase, and I-glutamyltransferase;
total, direct, and indirect serum bilirubin; and serum albumin.

Figure 1. Algorithm for the diagnosis of cirrhosis and chronic liver failure. (ALT = alanine transaminase; AST = aspartate
transaminase; CT = computed tomography; MRI = magnetic resonance imaging; CBC = complete blood count.)

Definitions and Etiologies
The liver aids greatly in the maintenance of metabolic
homeostasis by processing dietary amino acids, carbohy-
drates, lipids, and vitamins; metabolizing cholesterol and
toxins; producing clotting factors; and storing glycogen.
Injury to the liver parenchyma associated with an influx
of acute or chronic inflammatory cells is termed hepatitis.
Cirrhosis refers to a progressive, diffuse, fibrosing, nodu-
lar condition that disrupts the entire normal architecture
of the liver (Figures 2 through 4; Table 1).3,4 Fibrosis

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Cirrhosis and Chronic Liver Failure—Part I
Figure 2. Inferior surface of liver, biliary tree, and gallblad-
der (gross) revealing normal hepatic tissue and structure.
Figure 3. Inferior surface of liver and gallbladder (gross)
revealing cirrhotic liver.
previously was thought to be an irreversible scarring
process formed in response to inflammation or direct
toxic insult to the liver, but current evidence suggests that
fibrosis may be reversible in some patients with chronic
hepatitis B after antiretroviral therapy.8
Any chronic insult to the liver can cause progres-
sion to cirrhosis. Although numerous pathophysiologic
mechanisms of injury exist, the final common pathway
is persistent wound healing resulting in hepatic paren-
chymal fibrosis. In most persons, approximately 80 to
90 percent of the liver parenchyma must be destroyed
before liver failure is manifested clinically. When com-
plications of cirrhosis occur, they typically are related to
impaired hepatic function or actual physical disruption
and reorganization of the liver parenchyma.3
Clinical Presentation
HISTORY
Cirrhosis often is a silent disease, with most patients
remaining asymptomatic until decompensation occurs.
Physicians should inquire about risk factors that pre-
dispose patients to cirrhosis (Figure 1). Quantity and
758 American Family Physician www.aafp.org/afp
Figure 4A. Normal hepatic tissue (microscopic, 10X, tri-
chrome stain).
Figure 4B. Cirrhosis (microscopic, 10X, trichrome stain).
Photographs courtesy of Henry D. Appelman, M.D., Professor, Department
of Pathology, University of Michigan Medical School, Ann Arbor, Mich.
duration of alcohol consumption is an important fac-
tor in the early diagnosis of cirrhosis.3 Other risk fac-
tors include those for hepatitis B and C transmission
(e.g., birthplace in endemic areas, sexual history exposure
risk, intranasal or intravenous drug use, body piercing or
tattooing, accidental contamination with blood or body
fluids), as well as transfusion history and personal or
family history of autoimmune or hepatic diseases.3
Early and well-compensated cirrhosis can manifest as
anorexia and weight loss, weakness, fatigue, and even
osteoporosis as a result of vitamin D malabsorption and
subsequent calcium deficiency. Decompensated disease
can result in complications such as ascites, spontaneous
bacterial peritonitis, hepatic encephalopathy, and vari-
ceal bleeding from portal hypertension (discussed fur-
ther in part II2). Clinical symptoms at presentation may
include jaundice of the eyes or skin, pruritus, gastroin-
testinal bleeding, coagulopathy, increasing abdominal
girth, and mental status changes. Each of these clinical
findings is the result of impaired hepatocellular func-
tion with or without physical obstruction secondary to
cirrhosis. Because hepatic enzyme synthesis is required
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 Cirrhosis and Chronic Liver Failure—Part I
TABLE 1
Etiologies of Hepatic Cirrhosis

Most common causes

Alcohol (60 to 70 percent) for drug metabolism, heightened sensitivity and medi-
Biliary obstruction (5 to 10 percent) cation toxicity may occur in patients with impaired
Biliary atresia/neonatal hepatitis hepatic enzyme synthesis.3,9
Congenital biliary cysts
Cystic fibrosis PHYSICAL EXAMINATION
Primary or secondary biliary cirrhosis Physical examination of patients with cirrhosis may
Chronic hepatitis B or C (10 percent) reveal a variety of findings that should lead to a targeted
Hemochromatosis (5 to 10 percent) hepatic- or gastrointestinal-based work-up (Table 2).10
NAFLD (10 percent) —most commonly resulting from Many patients will already have had serologic or radio-
obesity; also can occur after jejunoileal bypass graphic tests or an unrelated surgical procedure that
Less common causes incidentally uncovered signs of cirrhosis.
Autoimmune chronic hepatitis types 1, 2, and 3 Most patients with cirrhosis severe enough to lead to
Drugs and toxins ascites have additional stigmata of cirrhosis on physical
Alpha-methyldopa (Aldomet) examination. Accurately diagnosing ascites depends
Amiodarone (Cordarone) upon the amount of fluid present in the abdomen,
Isoniazid (INH) the technique used to examine the patient, and the
Methotrexate patient’s habitus. The most useful physical finding in
Oxyphenisatin (Prulet)* confirming the presence of ascites is flank dullness to
Perhexiline*
Troglitazone (Rezulin)*
Vitamin A
TABLE 2
Genetic metabolic disease
G1-Antitrypsin deficiency Common Physical Examination Findings
Amino acid disorders (e.g., tyrosinemia)
in Patients with Cirrhosis
Bile acid disorders
Carbohydrate disorders (e.g., fructose intolerance, Abdominal wall vascular collaterals (caput medusa)
galactosemia, glycogen storage diseases) Ascites
Lipid disorders (e.g., abetalipoproteinemia) Asterixis
Porphyria Clubbing and hypertrophic osteoarthropathy
Urea cycle defects (e.g., ornithine carbamoyltransferase Constitutional symptoms, including anorexia, fatigue,
deficiency) weakness, and weight loss
Wilson’s disease Cruveilhier-Baumgarten murmur—a venous hum in patients
Idiopathic/miscellaneous with portal hypertension
Granulomatous liver disease (e.g., sarcoidosis) Dupuytren’s contracture
Idiopathic portal fibrosis Fetor hepaticus—a sweet, pungent breath odor
Indian childhood cirrhosis Gynecomastia
Polycystic liver disease Hepatomegaly
Infection Jaundice
Brucellosis Kayser-Fleischer ring—brown-green ring of copper deposit
Congenital or tertiary syphilis around the cornea, pathognomonic for Wilson’s disease
Echinococcosis Nail changes:
Schistosomiasis Muehrcke’s nails—paired horizontal white bands
Vascular abnormalities separated by normal color
Chronic, passive hepatic congestion caused by right-sided Terry’s nails—proximal two thirds of nail plate appears
heart failure, pericarditis white, whereas the distal one third is red
Hereditary hemorrhagic telangiectasia (Osler-Weber- Palmar erythema
Rendu disease) Scleral icterus
Veno-occlusive disease Vascular spiders (spider telangiectasias, spider angiomata)
Splenomegaly
NAFLD = nonalcoholic fatty liver disease.
Testicular atrophy
*—Not available in the United States.
Information from references 3 and 4. Information from reference 10.

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Cirrhosis and Chronic Liver Failure—Part I
percussion. When
Patients with numerous
this is detected, it
large vascular spiders are
is helpful to deter-
at increased risk for vari-
mine whether it
ceal hemorrhage.
shifts with rota-
tion of the patient
(shifting dullness) or whether it can be percussed
anteriorly. One study found absence of flank dullness
to be the most accurate predictor against the presence
of ascites; the probability of ascites without flank dull-
ness was less than 10 percent.11 Approximately 1,500 mL
of fluid must be present before dullness is detected on
physical examination, whereas routine ultrasonography
can detect as little as 50 mL of fluid in the abdomen.10
Vascular spiders (spider angiomata, spider telangiec-
tasias) are vascular lesions usually found on the trunk,
face, and upper extremities. Although their pathogenesis
is incompletely understood, it is believed that their pres-
ence in men is associated with an increase in the estra-
diol to free testosterone ratio.12 Vascular spiders are not
specific for cirrhosis: they also occur during pregnancy,
in patients with severe malnutrition, and in healthy
persons. The number and size of vascular spiders have
been shown to correlate with the severity of chronic liver
disease. Patients with numerous large vascular spiders
are at increased risk for variceal hemorrhage.13
Laboratory Evaluation
No serologic test can diagnose cirrhosis accurately.3 The
term liver function tests is a misnomer because the assays
in most standard liver panels do not reflect the function
of the liver correctly.10 Although liver function tests may
not correlate exactly with hepatic function, interpreting
abnormal biochemical patterns in conjunction with the
clinical picture may suggest certain liver diseases. When
a liver abnormality is suspected or identified, a liver
panel, a complete blood count (CBC) with platelets, and
a prothrombin time test should be performed.14 Com-
mon tests in standard liver panels include the serum
enzymes aspartate transaminase (AST), alanine trans-
aminase (ALT), alkaline phosphatase, and I-glutamyl-
transferase; total, direct, and indirect serum bilirubin;
and serum albumin. The ALT is thought to be the most
cost-effective screening test for identifying metabolic or
drug-induced hepatic injury, but like other liver function
tests, it is of limited use in predicting degree of inflamma-
tion and of no use in estimating severity of fibrosis.15 One
study found that a platelet count of less than 160 K per
mm3 has a sensitivity of 80 percent for detecting cirrhosis
in patients with chronic hepatitis C.16
A prospective study showed a strong correlation
760 American Family Physician www.aafp.org/afp
between liver function test results elevated to greater
than twice the upper limit of normal for at least six
months and underlying liver disease proved by liver
biopsy.17 Additional serologic studies should be pursued
in such circumstances to evaluate for various etiologies
of cirrhosis (Table 3).14,15,18,19 If clinical suspicion for liver
disease is high, then further serologic work-up is war-
ranted within six months.15 If a patient has a persistently
increased ALT level, viral hepatitis serologies should be
assayed. If these are negative, the remaining serologic
work-up should include an antinuclear antibodies test or
anti–smooth muscle antibody test, or both, to evaluate
for autoimmune hepatitis; and a fasting transferrin satu-
ration level or unsaturated iron-binding capacity and fer-
ritin level18 to evaluate for hereditary hemochromatosis.15
In patients younger than 40 years in whom Wilson’s dis-
ease is suspected, serum ceruloplasmin and copper levels
should be measured,19 but screening all patients with
chronic hepatic injury for Wilson’s disease is not indi-
cated.15 Primary biliary cirrhosis or primary sclerosing
cholangitis should be suspected in patients with chronic
cholestasis. Testing for G1-antitrypsin (A1AT) deficiency
may be of benefit in patients with chronic hepatic injury
and no other apparent cause. Although the role of A1AT
deficiency in liver disease in adults is not clearly defined,
testing is especially important in neonates with evidence
of hepatic injury.15 Ultrasonography or biopsy is neces-
sary to establish the diagnosis of NAFLD.
Radiographic Studies
Although various radiographic studies may suggest the
presence of cirrhosis, no test is considered a diagnostic
standard.3 The major use of radiographic studies is to
detect ascites, hepatosplenomegaly, hepatic or portal vein
thromboses, and hepatocellular carcinoma, all of which
strongly suggest cirrhosis.
ULTRASONOGRAPHY
Abdominal ultrasonography with Doppler is a nonin-
vasive, widely available modality that provides valuable
information regarding the gross appearance of the liver
and blood flow in the portal and hepatic veins in patients
suspected to have cirrhosis. Ultrasonography should be
the first radiographic study performed in the evaluation
of cirrhosis because it is the least expensive and does not
pose a radiation exposure risk or involve intravenous
contrast with the potential for nephrotoxicity as does
computed tomography (CT). Nodularity, irregularity,
increased echogenicity, and atrophy are ultrasonographic
hallmarks of cirrhosis. In advanced disease, the gross
liver appears small and multinodular, ascites may be
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 Cirrhosis and Chronic Liver Failure—Part I
TABLE 3
Clinical Laboratory Studies Used in Diagnosing Chronic Liver Disease

Etiology Laboratory tests and results

Alcoholic liver disease AST:ALT ratio > 2*

G1-Antitrypsin deficiency
Autoimmune hepatitis (type 1)
Chronic hepatitis B
Chronic hepatitis C
Hepatocellular carcinoma
Hereditary hemochromatosis
Nonalcoholic fatty liver disease
Primary biliary cirrhosis and
primary sclerosing cholangitis
Wilson’s disease
Elevated GGT
Decreased serum G1-antitrypsin
Genetic screening recommended in equivocal cases
Positive ANA and/or ASMA in high titer
Positive HBsAg and HBeAg qualitative assays
Once HBeAg is negative and HBeAb is positive, HBsAg should be monitored periodically to
determine viral clearance.
Hepatitis B virus DNA quantification used to document viral clearance
Elevated AST and/or ALT*
Positive hepatitis C virus antibody qualitative assay
HCV RNA quantification used to document viral clearance
HCV viral genotype to determine potential response to antiretroviral therapy
Elevated AST and/or ALT*
Elevated alpha fetoprotein, AST, and/or ALT*
Elevated ALP with obstruction or cholestasis
Elevated fasting transferrin saturation, unsaturated iron-binding capacity, or ferritin. A
transferrin saturation r 45 percent or an unsaturated iron-binding capacity 155 mcg per dL
(27.7 µmol per L) should be followed by analysis for HFE (hemochromatosis) gene mutations.
Elevated AST and/or ALT*
Ultrasonography or biopsy necessary to establish diagnosis.
Diagnosis made via contrast cholangiography, can be supported clinically by positive
antimitochondrial antibody (primary biliary cirrhosis) or antineutrophil cytoplasmic antibody
(primary sclerosing cholangitis) in high titers.
Elevated AST, ALT, and ALP common
Serum ceruloplasmin < 20 mg per dL (200 mg per L) (normal: 20 to 60 mg per dL [200 to 600
mg per L]), or low serum copper level (normal: 80 to 160 mcg per dL [12.6 to 25.1 µmol per L])
Basal 24-hour urinary copper excretion > 100 mcg (1.57 µmol) (normal: 10 to 80 mcg
[0.16 to 1.26 µmol])
Genetic screening recommended in equivocal cases, but must be able to detect multiple
mutations in Wilson’s disease gene.

AST = aspartate transaminase; ALT = alanine transaminase; GGT = I-glutamyltransferase; ANA = antinuclear antibody; ASMA = anti–smooth muscle antibody;
HBsAg = hepatitis B surface antigen; HBeAg = hepatitis B e antigen; HBeAb = hepatitis B e antibody; HCV = hepatitis C virus; ALP = alkaline phosphatase.
*—AST and ALT levels may be normal in advanced disease.
Information from references 14, 15, 18, and 19.

detected, and Doppler flow can be significantly decreased
in the portal circulation. The discovery of hepatic nod-
ules via ultrasonography warrants further evaluation
because benign and malignant nodules can have similar
ultrasonographic appearances.20 A study using high-
resolution ultrasonography in patients with cirrhosis
confirmed with biopsy or laparoscopy found a sensitiv-
ity and specificity for cirrhosis of 91.1 and 93.5 percent,
respectively, and positive and negative predictive values
of 93.2 and 91.5 percent, respectively.21
C T AND MRI
CT and magnetic resonance imaging (MRI) generally
are poor at detecting morphologic changes associated
with early cirrhosis, but they can accurately demon-
strate nodularity and lobar atrophic and hypertrophic
changes, as well as ascites and varices in advanced disease.
Although MRI sometimes differentiates among regener-
ating or dysplastic nodules and hepatocellular carcinoma,
it is best used as a follow-up study to determine whether
lesions have changed in appearance and size.20 CT portal
phase imaging can be used to assess portal vein patency,
although flow volume and direction cannot be deter-
mined accurately.22
Although used rarely, magnetic resonance angiography
(MRA) can assess portal hypertensive changes including
flow volume and direction, as well as portal vein throm-
bosis.22 One study reported that MRI can accurately

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Cirrhosis and Chronic Liver Failure—Part I
diagnose cirrhosis and provide correlation with its sever-
ity.23 Despite the potential of MRI and MRA in the
diagnosis and evaluation of patients with cirrhosis, their
widespread use is limited by their expense and by the
ability of routine ultrasonography with Doppler to obtain
adequate information for the diagnosis of cirrhosis and
presence of complications.
Liver Biopsy
Referral for liver biopsy should be considered after a thor-
ough, noninvasive serologic and radiographic evaluation
has failed to confirm a diagnosis of cirrhosis; the benefit of
biopsy outweighs the risk; and it is postulated that biopsy
will have a favorable impact on the treatment of chronic
liver disease. The sensitivity and specificity for an accurate
diagnosis of cirrhosis and its etiology range from 80 to
100 percent, depending on the number and size of the
histologic samples and on the sampling method.24
Liver biopsy is performed via percutaneous, transjugu-
lar, laparoscopic, open operative, or ultrasonography- or
CT-guided fine-needle approaches. Before the procedure,
a CBC with platelets and prothrombin time measure-
ment should be obtained. Patients should be advised to
refrain from consumption of aspirin and nonsteroidal
anti-inflammatory drugs for seven to 10 days before the
biopsy to minimize the risk of bleeding.
The Authors
JOEL J. HEIDELBAUGH, M.D., is a clinical assistant professor in the
Department of Family Medicine at the University of Michigan Medical
School in Ann Arbor, and medical director of the Ypsilanti (Mich.) Health
Center. He attended the State University of New York Health Science
Center at Syracuse and completed his residency training at St. Joseph’s
Hospital Health Center, Syracuse.
MICHAEL BRUDERLY, M.D., is a resident physician in the Department of
Family Medicine at the University of Michigan Medical School, where he
also received his degree.
Address correspondence to Joel J. Heidelbaugh, M.D., Ypsilanti Health
Center, 200 Arnet, Suite 200, Ypsilanti, MI 48198 (e-mail: jheidel@
umich.edu). Reprints are not available from the authors.
Author disclosure: Nothing to disclose.
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